Mechanism of Steatorrhea After Terminal Ileal Resection
Steatorrhea after terminal ileal resection occurs primarily through bile acid depletion causing fat maldigestion, with the severity directly related to the length of ileum removed. 1
Primary Mechanism: Bile Acid Depletion
The terminal ileum is responsible for reabsorbing more than 90% of bile acids through active uptake mechanisms. 1 When more than 60-100 cm of terminal ileum is resected, the loss of absorptive surface area cannot be compensated by increased hepatic synthesis of bile salts. 1 This creates a critical shortage of bile acids needed for fat emulsification and absorption.
The Two-Phase Pathophysiology
The mechanism differs based on resection length:
Small ileal resections (<100 cm):
- Decreased bile acid reabsorption leads to excess bile acids reaching the colon 1
- These unabsorbed bile acids cause osmotic diarrhea and mild fat malabsorption (typically <20 g/day steatorrhea) 2
- Fat digestion remains relatively preserved because sufficient bile acids are still produced 2
Large ileal resections (>100 cm):
- Severe bile acid depletion occurs because hepatic synthesis cannot keep pace with fecal losses 1, 2
- Aqueous phase bile acid concentrations drop significantly during digestion 2
- Approximately half of available bile acids precipitate intraluminally during digestion, further reducing their availability 2
- This profound fat maldigestion combines with reduced absorptive surface area to cause severe steatorrhea (>20 g/day) 3, 2
Secondary Contributing Mechanisms
Accelerated intestinal transit:
- Loss of the ileocecal valve and terminal ileum accelerates transit time 3
- Rapid transit prevents complete digestion and absorption of nutrients 3
- This creates an osmotic diarrhea component as undigested food particles retain water and electrolytes 3
Bacterial deconjugation:
- Excess bile salts reaching the colon undergo bacterial deconjugation 1, 4
- Deconjugated bile acids are less effective for fat absorption 4
- In patients with bacterial overgrowth of the small intestine, premature deconjugation worsens fat maldigestion 4
Colonic secretory effects:
- Unabsorbed bile salts and fatty acids presented to the colon decrease water absorption 3
- These substances stimulate active chloride and water secretion, producing a cholera-like secretory diarrhea 3
- This mixed secretory-osmotic mechanism amplifies the diarrhea beyond simple fat malabsorption 3
Critical Clinical Pitfall: The Cholestyramine Paradox
In severe bile acid malabsorption with established steatorrhea, cholestyramine can paradoxically worsen fat malabsorption. 1, 5 While cholestyramine effectively treats bile acid diarrhea in patients with small resections and mild malabsorption, it further depletes the already insufficient bile acid pool in patients with large resections. 1, 6 This creates a therapeutic dilemma where the standard treatment for bile acid diarrhea exacerbates the underlying steatorrhea.
Anatomical Reserve Concept
Patients with sufficient remaining small intestine can compensate for fat maldigestion by utilizing the distal small bowel more efficiently. 2 When cholestyramine was experimentally given to patients with small resections to induce fat maldigestion similar to large resection patients, their steatorrhea increased only minimally because they retained adequate absorptive capacity. 2 This explains why severe steatorrhea predominantly occurs when both fat maldigestion AND reduced surface area coexist. 2
Associated Complications
Hyperoxaluria and kidney stones:
- Fat malabsorption causes fatty acids to bind intestinal calcium 1, 7
- This leaves oxalate unbound and available for colonic absorption 1, 7
- Urinary oxalate excretion directly correlates with fecal fat excretion 1, 7
- The intact colon is essential for this complication—patients with jejunostomy do not develop hyperoxaluria 1, 7
Cholelithiasis: